To investigate the role of extracellular Cyclophilin A (eCypA) in neuroinflammation and blood-brain barrier (BBB) injury in acute ischemic stroke (AIS).
Approach:
Key Findings:
eCypA levels were significantly elevated in the serum of AIS patients and in tMCAO rat models compared to healthy controls.
C46 peptide administration resulted in changes in neurological function, cerebral infarct volume, and BBB permeability in tMCAO rats.
C46 administration preserved tight junction protein levels and inhibited microglial activation and proinflammatory mediator expression.
Interpretation:
Limitations:
The study involved a limited number of AIS patients and animal models.
Further research is needed to fully elucidate the mechanisms by which eCypA contributes to neuroinflammation and BBB damage.